The heart has a left side and a right side, each side including an atrium and a ventricle. The atria receive blood returning through veins to the heart and the ventricles pump blood away from the heart, through arteries, to circulate blood through the body. The blood returns to the right side of the heart through the venous system. The heart also includes four one-way valves (aortic, pulmonary, mitral and tricuspid) that function to maintain unidirectional blood flow as the heart contracts in a pumping stroke (systole) and then relaxes and expands to fill the ventricles (diastole). Each side has an A-V valve (the tricuspid and mitral valves) that controls flow from its atrium to its associated ventricle, and each ventricle has an output valve (the pulmonary valve and aortic valve). When the heart muscle contracts (systole) blood is pumped from both ventricles through their respective output valves. Oxygenated blood from the left ventricle is pumped through the aortic valve to the aorta and branching arteries while blood from the right ventricle is pumped through the pulmonary valve to the lungs where it is oxygenated. The oxygenated blood from the lungs is returned to the heart and is received in the left atrium. The right atrium receives return blood via the venous system. During diastole, blood in each atrium is drawn through its associated A-V valve to refill its associated ventricle in readiness for the next cardiac contraction.
In a healthy, properly functioning heart the A-V valves close fully during systole to prevent backflow of blood from the ventricles to the atria as the ventricles contract. Each of the mitral and tricuspid valves is defined by an arrangement of leaflets flexibly attached to an annular supportive ring. The leaflets have free marginal edges that engage each other during systole to close the flow path between the atrium and its associated ventricle. The closed positions of the leaflets of the A-V valves are limited and defined by tendonous chordae that are attached, at one end, to papillary muscles in the lower portions of the ventricles and, at their upper ends, to the undersides of the leaflets of the A-V valves as suggested in FIG. 2. In a healthy heart, the lengths of the chordae limit the movement of the leaflets during systole so that as the blood pressure in the ventricle increases, the free, marginal edges of the leaflets engage each other to close the valve and prevent backflow from the ventricles to the atria. During diastole the leaflets are not restrained by the chordae and their marginal edges are free to separate to allow blood flow from the atria to the associated ventricle.
Various cardiac-related diseases, however, may affect the heart by distorting its shape such that the leaflets of the mitral (left side) or tricuspid (right side) valve may not close properly and may result in backflow during systole. Deformation in the shape or structure of the heart wall may effect a change in the relative position of the papillary muscles to which the chordae are attached. That, in turn, affects the positions of the valve leaflets so that they may not close fully during systole. For example, such heart muscle deformation may occur in patients with coronary artery disease or those who have had myocardial infarction (heart attack) and are prone to developing mitral valve regurgitation due to chordal tethering, which results in reduced cardiac efficiency. That, in turn, may lead to further cardiac complications such as enlargement of the atria and/or ventricles, pulmonary hypertension, heart failure and other problems. Various procedures and techniques have been employed and proposed to improve the functioning of a compromised A-V valve. These include, for example, complex, invasive, open-heart surgery to surgically repair the valve, as by reforming or reinforcing the shape of the annulus of the valve or by selectively attaching portions of the marginal edges of leaflets together. Other remedies may involve replacement of an A-V valve with a mechanical valve or a bioprosthetic valve. Less invasive, catheter-based procedures also have been proposed, including adjustment of the chordae of the mitral or tricuspid valve. It is among the objects of the invention to provide catheter-based devices to facilitate minimally invasive adjustment of the length of chordae of A-V valves in order to adjust the closed position of the leaflets of the valve and restore the function to a malfunctioning A-V valve.